Sports Medicine

Gerard A. Malanga

Jose A. Ramirez-Del Toro

Jay E. Bowen

Joseph H. Feinberg

Garrett S. Hyman

Physiatric involvement in the field of sports medicine has greatly increased over the past two decades. More and more physical medicine and rehabilitation specialists are serving as team physicians at the high school, collegiate, Olympic, and professional levels. In addition, there has been increased involvement in the American College of Sports Medicine as participants and presenters. The Physiatric Association of Sports, Spine and Occupational Rehabilitation continues to promote and actively participate in educational programs dealing with sport medicine. It is encouraging that more physiatrists are publishing articles related to sports medicine, thus increasing Physical Medicine and Rehabilitation’s contribution to the literature. Validation of the effectiveness of non-operative treatment of various sports injuries will continue to substantiate the role of physiatrists as leaders in the area of sports medicine.

The primary purpose of this chapter is to review selected concepts pertaining to the treatment of sports injuries. The evaluation and treatment of some common injuries are also presented. Overuse injuries are discussed in a separate chapter in this textbook. The reader should understand that the area of sports medicine is broad; therefore, for those interested in treating sports injuries, additional reading of current textbooks and journals is essential. In addition, clinical experience gained through preparticipation physical examinations, sports clinics, and on-field coverage is invaluable to anyone who desires to care for injured athletes.

Since the previous edition of this book was published in 2005, a team physician consensus statement was developed. In a collaborative effort by six professional organizations—American Academy of Family Physicians, American Academy of Orthopedic Surgeons, American Academy of Sports Medicine, American Medical Society for Sports medicine, American Orthopedic Society for Sports Medicine, and American Osteopathic Academy of Sports Medicine—a consensus statement was devised that outlined the most important elements of sports medicine and their specific issues in injury and illness prevention (1). This chapter addresses every topic discussed in that consensus statement, and thus it is completely up to date in its information at the time of this meeting. Much of the previous edition was left intact, and new contributions have been included on the subjects of cardiovascular issues in sports and on anterior cruciate ligament (ACL) injury prevention.

TEAM APPROACH TO THE INJURED ATHLETE

Various health care professionals are involved in the care of injured athletes. Medical specialties traditionally involved in the care of athletes include physiatry, orthopedic surgery, internal medicine, family practice, emergency medicine, and pediatrics. Additional important team members include podiatrists, athletic trainers, therapists, nutritionists, and strength and conditioning specialists. The concept of working within a team approach is inherent in physiatry. During residency training and in practice, physiatrists continually coordinate care by interacting with physical therapists, occupational and speech therapists, psychologists, and other pertinent individuals. Although the vast majority of athlete symptoms are musculoskeletal in nature, a variety of problems can arise, ranging from skin disorders to cardiac symptoms. In addition, most acute injuries do not require operative intervention. A well-trained physiatrist would appear to be the most logical choice to direct the sports medicine team, addressing the majority of the nonoperative injuries in conjunction with athletic trainers, therapists, and others, and referring other conditions as needed to the most appropriate specialist in a timely manner.

BASIC TISSUE PHYSIOLOGY

Skeletal Muscle

Muscle constitutes the largest tissue mass in the body, comprising 40% to 45% of the total body weight. Muscles originate either from bone or dense connective tissue and are connected to these tissues by either the muscle itself or associated tendons. The muscle-tendon unit will cross one or more joints to its site of insertion, typically on bone. Those muscles that cross one joint are usually located close to bone and are generally involved in postural activities. One-joint muscles possess a slower contraction speed with increased force production. Examples of one-joint muscles include the vastus medialis/lateralis/intermedius of the quadriceps group and the soleus. In contrast to the one-joint muscles, those muscles that cross two or more joints are located more superficially and exhibit faster contraction speeds with relatively reduced force production. Examples of two-joint muscles include the biceps brachii and the gastrocnemius. Muscles can generate and attenuate force on a limb and stabilize a joint when firing synergistically with larger muscles.

Muscle that is torn has a limited ability to regenerate and often heals by dense scar formation. It has been reported that aging muscle demonstrates a decrease in size, number of muscle fibers (type II), and the number of motor units (alpha motor neuron and the muscle fibers it innervates). There is, however, no decrease in metabolic potential for aerobic and anaerobic activities with aging (2). Petrofsky and Lind (3) demonstrated little change in mean handgrip in men aged 22 to 62 years. Vandervoort and McComas found little change in dorsiflexion and plantar flexion torques between men aged 20 to 60 years, with a marked reduction in strength from age 60 to 100 years (4). Frontera (5) strength-trained men between 60 and 70 years and showed 107% and 226% strength increase for knee flexors and extensors. Fiatarone et al. (6) strength-trained nonagenarians, which resulted in a 174% increase in quadriceps strength and a 48% increase in gait speed. These studies demonstrate that muscular strength can be retained until very late in life, thereby supporting the concept that muscle loss with aging is primarily due to disuse more than age-related muscle fiber loss.

Tendons

As previously mentioned, a tendon is the structure that connects muscle to bone. Tendons consist of dense, regularly arranged collagen fibers meshed with elastin and a proteoglycan/glycosaminoglycan ground substance. The primary function of the tendon is to transmit the force generated in muscle to the bone. This process allows for the generation of movement of the extremities. The tendon is surrounded by a glistening, synovial-like membrane called the epitenon. The epitenon is continuous on its inner surface with the endotenon, a thin layer of connective tissue that contains lymphatics, blood vessels, and nerves. In some tendons, the epitenon is surrounded by a loose connective tissue called the paratenon. The paratenon functions as an elastic sheath that permits free movement of the tendon against surrounding tissue. The blood supply of tendons is variable and is compromised at sites of friction, torsion, or compression. Tendons with a blood supply that is frequently compromised include the supraspinatus, Achilles, and tibialis posterior. Tendons subjected to large, repetitive stresses can tear, become inflamed, or degenerate.

The aging process is associated with an increase in collagen cross-linkages, causing the fascia, ligaments, and tendons to be less distensible. Activity promotes connective tissue hypertrophy, whereas inactivity leads to atrophy. Physical activity also enhances the rate of collagen turnover, which shortens its life span. This turnover retards the effect of maturation of collagen cross-linkages and makes collagen more distensible (7).

Cartilage

Cartilage requires mechanical loading and unloading to remain healthy. This helps maintain nutrition to the tissues. Cartilage rarely has a direct blood supply and derives most of its nutrition via diffusion. If deprived of bearing weight, the cartilage undergoes degeneration (8). With repetitive overuse, cartilage can break down over time and lead to symptoms such as pain.

Ligaments

Ligaments are composed of approximately 70% collagen, along with ground substance and a larger percentage of elastin than tendons. They typically attach bone to bone and are important stabilizers of joints. Ligaments contain minimal blood supply, with most supplied by periarticular arterial plexuses. For example, the ACL, the main stabilizer of the knee against anterior translation of the tibia, has minimal intrasubstance arterial supply. The ACL does, however, receive some nutrition from the synovial fluid as well. The poor blood supply to ligaments explains the poor healing response in complete/partial injuries. The principles of collagen cross-linkages described in the tendon also apply to ligaments. Ligaments function to stabilize joints in concert with normal osseous alignment and musculotendinous stability. Ligaments also enhance proprioception via neurosensory receptors.

Bone

Bone is a dynamic tissue that remodels in response to external stress. Bone remodeling/healing represents the spectrum of bone’s response to stress (Wolff’s Law). Bone is a hard tissue consisting of cells in a matrix of ground substance and collagen fibers. The fibers are impregnated with mineral substance, chiefly calcium phosphate and carbonate. In addition to failure of bone secondary to repetitive stress (i.e., stress fractures), bony malalignment will also predispose the athlete to injury. Examples of malalignment include valgus alignment of the knee predisposing to patellar maltracking or a cavus foot predisposing to Achilles tendinitis.

BASIC PRINCIPLES OF NONOPERATIVE FUNCTIONAL REHABILITATION

Several basic principles can be applied to almost any acute sports injury, as outlined in Table 53-1. These rehabilitation phases provide a stepwise approach to treat and assess the progress of an athlete with an acute injury. Immobilization is avoided as much as possible because of its multiple detrimental effects on tissue healing (e.g., scar formation, contracture, and atrophy).

Phase I: Decrease Pain and Control Inflammation

The initial phase of treatment is to control the inflammatory reaction that occurs after an acute injury and its associated
pain, which inhibits muscle function. It should be noted that mediators involved in the inflammatory response are also important factors involved in the healing of soft-tissue injuries. Therefore, although the goal is to control the inflammatory response, eliminating it completely could be detrimental to tissue healing. The PRICE (protection, rest, ice, compression, elevation) approach is well known to those who care for athletes.

TABLE 53.1 Phases of Sports Rehabilitation

I. Resolving pain and inflammation

II. Restoring range of motion

III. Strengthening

IV. Proprioceptive training

V. Sports/task specific activities

Note: One should always remember to identify and address deficiencies along the entire kinetic chain.

After an injury, the area can be protected either by splinting, bracing, or taping/wrapping. It is very rare that any ligamentous or musculoskeletal injuries would require casting, which is usually avoided. Crutch ambulation (usually weight bearing as tolerated) for lower extremity injuries can be very helpful until a normal, pain-free gait pattern can be reestablished. Bracing should be limited to that which protects the specific area while allowing for full motion at other areas. It is often possible to use the same brace to facilitate early protective motion as well as return to functional activities later in the rehabilitation process (e.g., a double upright hinged knee brace following a medial collateral knee sprain).

Rest should be prescribed carefully, as it is important that the athlete does not become deconditioned during the rehabilitation of an injury. Fatigue results in a decrease in neuromuscular functioning and joint control, thereby placing greater dependency on the static stabilizers of joints (i.e., the ligaments), placing them at greater jeopardy for injury. Therefore, the proper term is relative rest, which means that while the affected area is rested, the remainder of the body is exercised. In particular, cardiovascular conditioning must be maintained. This can be done by alternative exercises that allow for protection of the injured area while stressing the cardiovascular system at the same intensity, duration, and frequency as the athlete had previously trained. For example, a running athlete who suffers a lower extremity injury that must be unloaded can use deep-water vest running at the same intensity level as before the injury. This has allowed athletes to maintain their cardiovascular fitness level while their injuries heal, allowing for safe return to play at close to the preinjury level and possibly prevent additional injuries.

Ice controls the initial inflammatory response and facilitates pain control immediately following an injury. The affected areas should be generally iced 20 minutes four to five times a day, or more often if possible. Ice is used for its properties of vasoconstriction, which limits the edema as well the release of vasoactive and pain factors, such as bradykinins and leukotrienes. Ice also can decrease conduction along pain fibers and act as a counterirritant to assist in pain control and to reduce muscle spasm. There are various methods of icing that include ice pack, ice massage, ice immersion, and devices that combine both ice and compression.

Compression is also used in an effort to limit the edema in the injured area. Ace wrapping is often used but can be problematic because of the difficulties in getting uniform or gradient (from distal to proximal) compression. A compressive stockinette (e.g., Tubigrip) can be very helpful in this regard. A sleeve can be cut to whatever size is necessary and simply applied. For additional compression, it can be folded over onto itself. Care must be taken to avoid excessive pressure over bony protuberances or superficial nerves. Compressive braces can also be effective (e.g., air splints for ankle sprains). Finally, devices that combine icing with compression have been found to be very useful and effective in the postinjury as well as postoperative rehabilitation of athletic injuries. They can be used not only by therapist and athletic trainers but also at home by motivated athletes.

Elevation is yet another means to control postinjury swelling. The injured limb should be elevated above the level of the heart to optimally assist with venous and lymphatic drainage and therefore control edema. Keeping the lower extremities out of a dependent position is helpful as well in limiting the pooling of inflammatory and posttraumatic products.

Additionally, nonsteroidal antiinflammatory drugs (NSAIDs) for a short period of time, if not contraindicated, and electrical stimulation can assist with both inflammation and pain control. Whether they offer clear advantages over using just the above program is a matter of debate, but if available and not contraindicated, appear reasonable.

Phase II: Restore Normal/Symmetric Range of Motion

Pain and swelling can inhibit motion or produce altered motor patterns that, if established, often require retraining to restore proper motor control. An example is an athlete with an antalgic gait following a knee or ankle injury. This movement pattern must be discouraged while the area is gradually mobilized. Immobility will result in scar and contracture and therefore is not recommended. Range of motion (ROM) allows for controlled stress to a joint, which will stimulate proper collagen deposition. Motion provides sensory input to the central nervous system, which stimulates the proprioceptive system as well as modulates pain via the Gate theory. In the early phase, pain-free movement of a joint and stretching that prevents contractures are encouraged as the motion that results in stress on the injured area is avoided. As the pain and inflammation subside, more aggressive stretching and mobilization continue until symmetric (to the unaffected limb) motion is achieved with normal movement patterns.

Phase III: Restore Normal/Symmetric Strength

Strengthening a painful, inflamed limb that lacks normal ROM can result in further problems that can delay recovery from injury. Therefore, a stepwise approach toward strengthening must be used. In the early postinjury phases, pain-free isometric contractions performed several times throughout the day are encouraged in an effort to retard muscular atrophy. A simple method is to recommend 10-second contractions, with 10 repetitions, 10 times a day. These isometric contractions may need to be performed through multiple angles as the strengthening is specific to the manner and position in which a muscle is trained. As the injured area recovers and ROM is restored, isotonic strengthening can begin if possible. Currently, there is no significant role for isokinetic strengthening because of poor functional
carryover. To that end, closed kinetic chain exercise should begin as soon as possible and progressed as able. Resistance training can be in the form of exercising against gravity, free weights machines, and resistance tubing. The strengthening should be as functional as possible, attempting to match the demands of the sport. Resistance tubing strengthening is attractive because of its ease and simplicity; however, the greatest tension with resistance occurs at the end ROM, where the muscle is usually weakest and the joint is most vulnerable. Therefore, this should be reserved for later stages of the strengthening program. In addition, the use of plyometric exercise should be included as the athlete is preparing to return to sport, because such training may ready the athlete for explosive bursts that are often a necessary part of many high demand sports.

Phase IV: Neuromuscular Control (Proprioceptive) Retraining

In order to dynamically control a joint during sport activity, there needs to be not only full ROM and normal strength but also adequate dynamic motor control. Specifically, the injured joint needs to be stabilized by synchronous activation of appropriate muscle groups so that the larger, more powerful muscles may safely produce the necessary force required in sports activity. Many injuries can result in proprioceptive loss that may predispose an athlete to repeat injury. As in other areas addressed in the rehabilitation process, the proprioceptive system needs to be progressively challenged in order for progress to be made. Simple proprioceptive training can include seated exercises with a wobble board for lower extremity injuries or loading exercises of the arm either on a table or wall. As the athlete recovers, and assuming that there is near full ROM and strength, the proprioceptive system is progressively challenged (e.g., balancing on a single leg while catching and throwing, balancing with eyes closed). Proprioceptive training requires a great deal of one-on-one work with a therapist or trainer and often creativity in developing ways to challenge the proprioceptive system that corresponds to the athlete’s sport (9).

Phase V: Return to Sport Activities

As the athlete completes these phases, the therapist or trainer must then begin the transition to return to sport. This occurs as the athlete successfully meets the challenges of the previous phases. The athlete then is put through activities that replicate the demands of the sport. For example, a basketball player will be given various drills that include running, cutting, and jumping (and landing) using optimal biomechanics. Once the athlete demonstrates that he or she can successfully negotiate the various drills and challenges that will occur in the sport in a controlled situation, then it should be clear to everyone on the team (including the athlete) that he or she can safely return to their sport.

CARDIOVASCULAR ISSUES IN SPORTS

An integral part of the preparticipation physical examination for athletes is the cardiovascular evaluation. The goal of this evaluation is to identify athletes who are at risk for sudden cardiac death during vigorous physical activity. By applying elements of the personal history, the family history, and the physical exam, the most important signs and symptoms of the most common cardiac reasons for sudden death can be obtained. These include hypertrophic cardiomyopathy (HCM), selected arrhythmias, coronary artery anomalies, ruptured aortic aneurysms, and commotion cordis (1). In particular, HCM has received much attention in the press and in the literature as it has taken the lives of several high profile athletes. It is the primary cause of sudden atraumatic death in athletes, responsible for nearly 35% of those deaths (10). We will briefly discuss HCM below because it is important to understand the pathophysiology in order to be able to recognize the signs and symptoms of this silent killer.

Hypertrophic Cardiomyopathy

HCM is a hereditary condition that occurs as commonly as 1:500 in the adult population (11). It is most commonly transmitted via an autosomal dominant pattern in which there is a genetic defect in the sarcomere contractile proteins (12). This leads to an increased ventricular muscle mass that is characteristically the hallmark of this condition. It is important to note that there is not an associated increase in actual ventricular cavity size; just a hypertrophy of the muscle tissue itself. This is important because it can often be difficult to differentiate HCM from a conditioned athlete’s heart. A well-conditioned athlete can sometimes develop a structural remodeling and an increased ventricular cavity to accommodate the larger ejection fraction that develops due to their increased efficiency for oxygen extraction at the tissue levels, while at the same time maintaining normal systolic and diastolic function (11). In contrast, in HCM, there is a severe net reduction in actual inner ventricular cavity size because of the much enlarged and hypertrophied muscle mass.

In HCM, there is also evidence of reduced compliance secondary to the inability to adequately relax the hypertrophied muscle mass. This causes diastolic dysfunction, which in turn leads to an increased left ventricular end-diastolic pressure (LVEDP) and subsequent impedance to appropriate diastolic filling. This increase in LVEDP may then lead to the development of a pressure gradient between the left ventricle and the aorta. This gradient is clinically significant to the sports medicine physician because it can be affected with certain maneuvers aimed at increasing or decreasing left ventricular end-diastolic filling. Techniques such as Valsalva maneuver or changing positions from standing to squatting and back to standing are aimed at increasing or decreasing left ventricular end-diastolic filling. If a murmur is present, these techniques will affect the quality of the murmur differently depending on its etiology.

A systolic murmur can occasionally be heard in HCM. It is the result of the pressure gradient between the left ventricle and the aorta that was previously mentioned. Any maneuver that decreases left ventricular end-diastolic filling, such as Valsalva or rising from squatting to standing, will subsequently
lead to dynamic obstruction in the left ventricular outflow tract, thereby increasing the intensity of the HCM murmur. Conversely, the murmur is also ominous if it decreases in intensity when maneuvers to increase left ventricular end-diastolic filling are performed. Such maneuvers will alleviate dynamic obstruction in the left ventricle outflow tract, thus decreasing the murmur. Therefore, when a patient goes from standing to squatting and the murmur that the physician is hearing is decreased in intensity, this is a sign of abnormal hemodynamics and can cause the physician to be suspicious for HCM. Benign murmurs, on the other hand, will increase with squatting because blood return to the heart is increased; and they will decrease in intensity upon rising from squatting, as blood return to the heart diminishes (10).

The most common signs/symptoms of HCM are syncope or sudden cardiac death with exertion. Therefore, risk factors for HCM, as well as for all the other cardiovascular anomalies such as arrhythmias or ruptured aneurysms or coronary artery anomalies, must be understood and thoroughly investigated in the preparticipation physical exam evaluation.

General Cardiac Evaluations

The guideline recommendations for preparticipation athletic screening of the cardiovascular system include a thorough evaluation of the family history, the personal and present medical history, and the physical evaluation (13,14).

Importantly, one should ask if there is a history of premature or sudden cardiac death, or if there have been any deaths of unknown etiologies in young family members. As mentioned earlier, HCM is a familial disease, as is Marfan’s Syndrome, which can lead to ruptured aortic aneurysms. Thus, any history of prior sudden cardiac death, particularly in young family members, is imperative. It is also important to screen for history of heart disease in anyone in the family under the age of 50.

There are also elements of the personal history that are crucial to the cardiovascular evaluation of any athlete. Questions regarding medical history of heart murmurs can signify more than just a benign flow murmur. Likewise, systemic hypertension, particularly if it is not well controlled, can cause abnormal hemodynamics and add undue stress to the heart. The physician must also importantly inquire about exertional symptoms. Has the patient ever had exertional syncope or near syncope? Is there a history of exertional chest pain? Is there a history of dyspnea upon exertion that is out of proportion to the amount of exercise being performed? Have there been palpitations or irregular heartbeats? All of these could be symptoms of a heart that is struggling to meet the demands of the exercising musculoskeletal system (14,15).

The physical exam, as we have alluded to, is key to identifying possible at-risk athletes. Auscultation of a murmur warrants further evaluation and requires employment of the previously described tactics (Valsalva, squatting, standing) to be able to demonstrate the qualities of the murmur and to possibly define some pathology. Of course, any heart rhythm abnormality needs to be evaluated further. Pulses must be palpated for intensity and heart rhythm. Lateral and inferior migration of the point of maximal impact (PMI) of the heart on the chest wall may also be a sign of left ventricular hypertrophy. If any of the above-mentioned scenarios are uncovered, the athlete must be precluded from exercise until further workup has occurred with EKG, echocardiogram, and possibly a Holter monitor.

Interestingly, Corrado et al. performed a multiyear study in Italy, analyzing the efficacy of a nationally implemented standardized preparticipation cardiovascular evaluation for the detection of at-risk athletes for sudden death. Their study also included an EKG on top of all the previously described history and physical exam (16). This multiyear study concluded that there was decreased incidence of sudden cardiac deaths since the initiation of the national screening program secondary to better detection of the at-risk athletes and precluding them from participation. It prompted some here in the United States to ask questions about whether we need to have a national standardized preparticipation screening program, and if we do, should we add the EKG to the preparticipation evaluation as a routine screening test to complement the history and physical exam. However, there have been questions raised regarding true cost effectiveness and utility of the EKG as a part of the routine screening cardiac evaluation (17).

Needless to say, an aggressive and focused preparticipation evaluation must be an essential part of the armamentarium of the sports medicine physician. He or she must understand the pathophysiology of the most common causes of sudden cardiac deaths in athletes, as well as be able to identify which athletes are at risk for this based on their preparticipation evaluation. The physician must also serve as an educator to coaches, players, and parents about the warning signs of dangerous cardiac scenarios (1).

CONCUSSION IN SPORTS

A concussion results from trauma transmitted either directly or indirectly to the head, causing impairment of the brain’s normal function (Table 53-2). This impairment may last from seconds to days. At times, dysfunction or postconcussive symptoms (headache, dizziness, tinnitus, irritability, memory impairment, nausea/vomiting, fatigue, etc.) can last months to years. Concussion is a type of brain injury, which can be classified as minor, mild, moderate, or severe (18).

Documented signs and symptoms of a brain injury (concussion) include amnesia (retrograde/antegrade), loss of consciousness (LOC), headache, dizziness, nausea, attentional deficit, and blurred vision. Additional features have been mentioned and include confusion/disorientation, being “dazed” or having one’s “bell rung,” inability to relate games specifics (period, opponent, score, plays), dizziness, seeing flashing lights, tinnitus, diplopia, impaired concentration, slurred speech, inappropriate behavior (laughing/crying), irritability, altered taste or smell, impact seizure, imbalance, and decreased ability to play the sport (19).

TABLE 53.2 Concussion

Concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces.

Several common features that incorporate clinical, pathological, and biomechanical injury constructs that may be used in defining the nature of a concussive head injury include

1. Concussion may be caused by a direct blow to the head, face, neck, or elsewhere on the body, with an “impulsive” force transmitted to the head.

2. Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously.

3. Concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury.

4. Concussion results in a graded set of clinical syndromes that may or may not involve LOC. Resolution of the clinical and cognitive symptoms typically follows a sequential course.

5. Concussion is typically associated with grossly normal structural neuroimaging studies.

Source: Aubry M, Cantu R, Dvorak J, et al. Summary and agreement statement of the first international conference on concussion in sport, Vienna 2001. Recommendations for the improvement of safety and health of athletes who may suffer concussive injuries. Br J Sports Med. 2002;36(1):6-10; Aubry M, Cantu R, Dvorak J, et al. Summary and agreement statement of the first international conference on concussion in sport, Vienna 2001. Phys Sport Med. 2002;30(2):57-63.

The evaluation of the athlete suspected of a concussion should include a history of past head and neck injuries (including orofacial), severity of impact (magnitude of force, linear, rotational), prior structural deficits if the athlete had a prior injury, and genetic phenotype if known (apolipoprotein). This should be combined with the detailed evaluation of the current episode. Although LOC is an appropriate concern, it appears insensitive for most concussions, and amnesia may be a better measure of severity.

If a history of multiple concussions is obtained, care should be taken to quantify severity of the precipitating events and duration of concussive symptoms. It appears that a history of concussion results predisposes to subsequent brain injuries.

Postconcussive symptoms include headaches, nausea, vomiting, drowsiness, numbness or tingling, balance impairment, vertigo, sleep impairment, light or noise sensitivities, difficulty concentrating or remembering, sadness, anxiety, dizziness, irritability, or fatigue. Although postconcussive symptoms are controversial, they are felt to arise from either the direct brain impairment or a psychological reaction to the brain injury itself.

Concern for concussion should go beyond the immediate injury. If an athlete were to return to competition without being fully recovered, he or she could sustain a second injury of greater severity. Schneider first described such a syndrome in 1973 (20). It was later coined “second-impact syndrome” by Saunders and Harbaugh in 1984 (21). Second-impact syndrome results from a person sustaining a second brain injury before symptoms of a prior concussion have cleared. This second trauma can be relatively minor in severity and may not involve the head. It is believed that the brain’s vascular autoregulation becomes impaired from the first injury, leading to engorgement within the cranium. Increased intracranial pressure ensues, resulting in herniation of the medial temporal lobes through the tentorium or cerebellar tonsils through the foramen magnum. Clinically, the athlete suffers a second head injury and becomes dazed. Within 15 seconds to a couple of minutes, the athlete rapidly decompensates. He or she collapses, becomes semicomatose, and suffers from pupil dilation, loss of eye movements, and respiratory failure.

The precise incidence of second-impact syndrome is unknown, but from 1980 to 1993, only 35 presumed cases were reported to the National Center for Catastrophic Sports Injury Research in Chapel Hill, North Carolina. Seventeen of these cases were confirmed. The mortality rate is 50%, and the morbidity rate is 100% (22).

Impact seizures are an uncommon result of a mild head injury. They develop within seconds of the insult and are not associated with any structural brain injury or long-term risks. The seizures do not need treatment, and the athlete should not necessarily be eliminated from sport.

Concussions are more common in some sports, including American and Australian football, ice hockey, rugby, and soccer. The National Center for Catastrophic Sports Injury Research’s database compiles statistics on baseball, ice hockey, tennis, basketball, lacrosse, track, cross-country skiing, volleyball, field hockey, soccer, water polo, football, softball, wrestling, gymnastics, and swimming. Estimated annual incidence of concussions is approximately 300,000 in the United States. Concussion rates per 1,000 player hours range from 0.25 to 23.0 (23).

Many different scales have been developed to evaluate concussed athletes for research purposes (Cantu, Colorado, American Academy of Neurology, Virginia Neurological Institute, Torg, etc.). Each includes parameters of consciousness and amnesia with varying importance to determine the grade or severity of injury. Currently, posttraumatic amnesia or working memory is felt to be of greater importance than LOC. People have tried abbreviated sidelines psychological batteries (24), balance (25) and cerebellar physical examination maneuvers, and assistance from coaches and athletic trainers for return-to-play evaluation. Recent research with more sensitive instruments demonstrates impairment in conceptual thinking (26), sustained attention and visuoperceptual processing (27), and reaction time (28,29). Currently, clinicians have no scientifically validated information on clinical management of concussions or treatment effects on long-term outcomes, though studies are currently on-going.

Minor traumatic brain injury (TBI) has not been discussed in the literature as such. An athlete sustains a momentary loss or alteration in consciousness and has memory impairments that may be unrecognized. Often athletes are evaluated (usually football players), who show signs and symptoms of
a mild TBI when there has been no clear identifiable event. It is unclear whether their symptoms are the result of many “mini” concussions, one blow to the head they cannot recall, or repetitive acceleration-deceleration trauma to the head. These seemingly less severe concussions, in which no LOC occurs, may have greater long-term neurologic sequelae than a grade 2 concussion, in which a significant period of LOC exists. Further contributing to the difficulty in grading concussions is the underreporting of grade 1 concussions by the athlete. This occurs because of his or her fear of being withdrawn from the contest or because the athlete feels it is “part of the game.” Athletes commonly refer these milder concussions as getting the “bell rung.” One must question whether they are truly milder head injuries. This should be taken into consideration when evaluating an athlete. Studies are currently ongoing on this subject matter.

Mild head injury generally has no LOC, posttraumatic amnesia of less than 1 hour, and a Glasgow Coma Scale of 15 (30). The greatest number of concussions falls into this category of severity (including the “minor” TBI) (31). Because the Glasgow Coma Scale is not sensitive enough to be useful in the evaluation of a mild TBI, and LOC also appears to be too insensitive, more weight has been placed on amnesia.

Moderate TBIs generally have no LOC of less than 5 minutes, and posttraumatic amnesia from 1 to 24 hours, whereas severe TBIs have an LOC greater than 5 minutes and posttraumatic amnesia greater than 24 hours.

Paper-and-pencil testing (McGill ACE, SAC) and computerized evaluations (IMPACT, CogSport, etc.) are currently being researched (National Football League, National Hockey League, Australian football, Pennsylvania State University, University of Pittsburgh, etc.) in an attempt to develop a quick, simple, cost-effective, and accurate adjunct to the clinical evaluation for evidence-based decision making and return-to-play guidelines. Many of these are being implemented in the preseason as baseline tests in many high schools and universities around the country, with the goal being to retest an athlete after a concussion occurs. The athlete’s progress can be tracked based on his or her scores in these evaluations. This serves, as stated above, as an adjunct to the clinical evaluation for decision making regarding a return-to-play timeframe.

There had been no consensus regarding concussions or return to play until a conference was held in 2001 in Vienna (18) (Table 53-3). The consensus is that when an athlete is initially diagnosed with a concussion, he or she should not return to the current practice or game. He or she should have continued, intermittent monitoring for deterioration. There should be a medical evaluation if concern for a concussion was made by someone other than a physician. Return to play should be in a stepwise fashion, and if doubt is present, the athlete should be held from competition.

Return to play should include no postconcussive symptoms at rest or exertion, consideration or the concussion scales, and prior history of the athlete and his or her injuries. Some institutions have preparticipation neuropsychological batteries on athletes, which can be repeated and compared with themselves, as well as age-matched and position-matched controls. This can be a great assistance in the decision-making process.

TABLE 53.3 Concussion Guidelines from the 2001 Vienna Concussion in Sports Guidelines (CISG)

•	Revised definition
•	Strength and weakness of existing concussion guidelines (no singly system endorsed)
•	Absence of scientifically validated return-to-play guidelines
•	Defined signs and symptoms of acute concussion
•	Cognitive (confusion, amnesia, LOC, disorientation)
•	Symptoms (headache, dizziness, nausea, loss of balance, “dinged” or stunned, seeing stars of flashing lights, tinnitus or double vision, sleepiness, sleep disturbance, fatigue, slowness, etc.)
•	Signs (LOC/impaired consciousness, impaired coordination, impact seizure, gait abnormality, slow to answer or follow direction, distracted-poor concentration, inappropriate behavior, vomiting, vacant stare, slurred speech, personality change, poor game/practice play, etc.)
•	Neuropsychological testing is a cornerstone tool
•	Neuroimaging not essential for uncomplicated concussion
•	Research is ongoing and vital
•	Rehabilitation program essential
•	Return-to-play protocol (no activity until asymptomatic → light aerobic activity → sport-specific training → noncontact drills → full contact practice → game play → able to progress as long as asymptomatic)
•	Prevention—rule changes and enforcement of rules are vital
•	Education—promotion of fair and ethical play in sports
Adapted from Aubry M, Cantu R, Dvorak J, et al. Summary and agreement statement of the first international conference on concussion in sport, Vienna 2001. Phys Sport Med. 2002;30(2):57-63.

CERVICAL SPINE INJURIES IN SPORTS

Cervical spine—related injuries are relatively common in contact/collision sports, such as football and wrestling. These injuries can include trauma to the tissues of the neck, including the muscles, ligaments, discs, and bones, as well as the neurologic structures, such as the nerve roots and spinal cord.

Cervical Disc

As with the general population, cervical disc disease is seen in the more mature athlete. Some sports such as football and wrestling appear to increase the risk of developing a cervical disc syndrome. Cervical disc disease most commonly affects C5 to C6, followed by C6 to C7 and then C4 to C5. This pattern roughly corresponds to the amount of normal motion that occurs at each level, with areas of greater motion (i.e., C5
to C6) developing degeneration sooner. Some physicians have divided cervical disc disease into soft and hard disc diseases. The soft disc refers to an acute disc herniation, usually in a younger person with or without neurologic involvement, depending on the degree of mechanical or chemical irritation by the nucleus pulposus on the nerve root structures. The hard disc is the result of events occurring over time and the progressive decline in the cervical disc and surrounding structures resulting in spondylosis. This degeneration process is characterized by disc bulges, herniations, thickening of the posterior longitudinal ligament, thickening of ligamentum flavum, degeneration of the synovial facet joints, or osteophytes. These anatomic changes result in a greater likelihood of structural compromise or impaired spinal kinematics. These changes may result from the athletes’ sport or, as with the general population, chronic impaired loading through altered posture and inappropriate loading of the various spinal structures over time. Of specific note, radiographic changes correlate poorly with signs and symptoms that patients exhibit (Figs. 53-1, 53-2, 53-3) (32,33).

Cervical Cord Neuropraxia

Cervical cord neuropraxia results from an injury to the spinal cord presenting with complete transient paralysis, motor impairment, sensory changes, or a combination of these in at least two limbs. Transient quadriparesis is a rare cervical spine injury caused by axial loading of the neck in extension or flexion that results in nonpermanent complete sensory and motor impairment in all four limbs resolving in 10 minutes to 48 hours (34). One should remember that any neurologic impairment in more than one extremity is a central nervous system injury unless proven otherwise (sometimes referred to as burning hands syndrome). Obersteiner originally described this as a spinal cord concussion in 1879 (35). It has been estimated at 1.3 episodes per 10,000 athletes or an incidence of 6 h 10,000 athletes (36).

FIGURE 53-1. Good cervical posture—lateral view. The head is aligned over the cervical spine with maintained lordosis and normal structural loading.

It appears that this is a neuropraxic injury from local cord anoxia and increased intracellular calcium (37). During hyperextension, a “pincer” effect can occur, causing the posterior inferior aspect of the superior vertebra and anterior superior aspect of the inferior vertebra to produce a resultant compression of the spinal cord. In this position, the diameter can narrow up to 30% (38). With associated spinal degeneration, even greater compromise can occur.

In the event of either a significant head injury in which a concomitant neck injury may be present or isolated cervical injury, the medical team should be appropriately prepared by having the correct equipment available and having practiced the evaluation and treatment of the athlete with this type of injury. This includes the possibility of spine-boarding the athlete and removal of the athlete’s protective gear (i.e., facemask removal). An athlete who is wearing protective headgear (e.g., a helmet) with a suspected spinal injury should not have the helmet removed. It is imperative that the sideline physician understands how to protect the spine and coordinate spine-boarding and transportation of an athlete with a suspected spine injury.

In the evaluation of an athlete with suspected cervical disc disease, the location, referral pattern, quality of the symptom, and associated neurologic symptoms—such as Lhermitte’s sign, balance/gait abnormalities, limb weakness, or bowel/dysfunction—must be obtained. This should occur to determine if additional structures have been damaged. A complete physical examination (including cervical tenderness and ROM), a detailed neurologic examination of the
upper and lower limbs (including power, sensation, reflex assessment, and a Spurling’s maneuver), and evaluation for upper motor neuron signs (Hoffman, plantar responses, tone, etc.) are all necessary.

FIGURE 53-2. Poor cervical posture—lateral view. The head is protracted forward with extension of the occiput and loss of lordosis.

FIGURE 53-3. Cervical spine radiograph showing osteoarthritic changes—lateral view. Cervical osteoarthritis from chronic abnorma loading of the spinal elements (i.e., discs, facets, etc.).

X-rays may be helpful in evaluating the athlete for a fracture, spinal instability (with the use of flexion/extension views), osseous degeneration, or destructive lesions from tumor or infection. Anteroposterior, lateral, open-mouth, and oblique views should be the initial evaluation. If pain or neurologic signs persist or ROM has not returned, further imaging should be considered. Magnetic resonance imaging (MRI) is probably the study of choice if not contraindicated. A fat-suppressed image should be included to evaluate for ligamentous injury, especially when instability is seen on radiographs or clinically suspected. The spinal diameter and relative space can be evaluated. Normal midsagittal diameter on plain x-rays should be 14 to 23 mm. If the canal is less than 13 mm, it is considered stenosis (39).

Torg et al. introduced a ratio to assist with measuring and stratifying persons at risk for cervical cord neuropraxia from spinal stenosis (40

Only gold members can continue reading. Log In or Register to continue